The Affordable Care Act (ACA) was signed into law on March 23, 2010 and will fundamentally alter health care in the United States for years to come. The US is currently one of the only industrialized countries without universal health insurance. The new law expands existing public insurance for the poor. It also provides financial credits to low income individuals and some small businesses to purchase health insurance. By government estimates, the law will bring insurance to 30 million people. The law also provides for a significant new investment in prevention and wellness. It appropriates an unprecedented $15 billion in a prevention and public health fund, to be disbursed over 10 years, as well as creates a national prevention council to oversee the government's prevention efforts. This paper discusses 3 major prevention provisions in the legislation: 1) the waiving of cost-sharing for clinical preventive services, 2) new funding for community preventive services, and 3) new funding for workplace wellness programs. The paper examines the scientific evidence behind these provisions as well as provides examples of some model programs. Taken together, these provisions represent a significant advancement for prevention in the US health care system, including a shift towards healthier environments. However, in this turbulent economic and political environment, there is a real threat that much of the law, including the prevention provisions, will not receive adequate funding.
Health Care Reform/*legislation & jurisprudence ; Humans ; Insurance, Health/*legislation & jurisprudence ; Medicaid/legislation & jurisprudence ; Patient Protection and Affordable Care Act ; Preventive Health Services/*legislation & jurisprudence ; United States

To evaluate radiosensitivity and the effects of radiation on the expression of vascular endothelial growth factor (VEGF) and VEGF receptors in the canine oral melanoma cell line, TLM 1, cells were irradiated with doses of 0, 2, 4, 6, 8 and 10 Gray (Gy). Survival rates were then determined by a MTT assay, while vascular endothelial growth factor receptor (VEGFR)-1 and -2 expression was measured by flow cytometry and apoptotic cell death rates were investigated using an Annexin assay. Additionally, a commercially available canine VEGF ELISA kit was used to measure VEGF. Radiosensitivity was detected in TLM 1 cells, and mitotic and apoptotic cell death was found to occur in a radiation dose dependent manner. VEGF was secreted constitutively and significant up-regulation was observed in the 8 and 10 Gy irradiated cells. In addition, a minor portion of TLM 1 cells expressed vascular endothelial growth factor receptor (VEGFR)-1 intracellularly. VEGFR-2 was detected in the cytoplasm and was down-regulated following radiation with increasing dosages. In TLM 1 cells, apoptosis plays an important role in radiation induced cell death. It has also been suggested that the significantly higher VEGF production in the 8 and 10 Gy group could lead to tumour resistance.
Animals ; Apoptosis/*radiation effects ; Cell Line, Tumor/radiation effects ; Dogs ; Dose-Response Relationship, Radiation ; Enzyme-Linked Immunosorbent Assay/veterinary ; Melanoma/genetics/metabolism ; Mouth Neoplasms/genetics/metabolism ; Radiation Tolerance ; Tetrazolium Salts/metabolism ; Thiazoles/metabolism ; Up-Regulation/*radiation effects ; Vascular Endothelial Growth Factor A/genetics/metabolism/*radiation effects ; Vascular Endothelial Growth Factor Receptor-1/genetics/metabolism/*radiation effects ; Vascular Endothelial Growth Factor Receptor-2/genetics/metabolism/*radiation effects